Hypnosis was discovered by a Viennese physician, Friederich Anton Mesmer, in the late 1700's. Mesmer began with a theory about animal magnetism, involving the distribution of magnetic fluid within an organism's body. He used hypnosis, then called Mesmerism, to produce a more harmonious distribution of this magnetic fluid in the body. Mesmer immediately understood the implications of his work, as he immediately claimed mesmerism as a superior form in which to hinder the development of disease without exposing the patient to the more hazardous techniques of the time period. In 1784, Louis XVI formed a commission to investigate Mesmer's findings. The commission was, incidentally, headed by none other than Benjamin Franklin. Although Mesmer's findings on hypnosis were undisputed by the commission, the commission played down the effects of an unfounded "magnetic fluid" in the human body and attributed Mesmerism's effects to a placebo effect. Because of the commission's findings regarding magnetism, Mesmerism fell from popularity (Hall, 1986)

In England around 1843, the surgeon James Braid revisited the phenomenon of Mesmerism and renamed it hypnosis, after the Greek god of sleep, Hypnos. He was the first person to attribute the phenomenon to psychological rather than physical variables. His findings renewed interest in the subject, especially in France, where hypnosis gained popularity again as a form of pain reduction during surgery. Eventually, Braid's technique was found to be unsatisfactory, and hypnosis drifted out of favor once again (Hall, 1986).

In the late 1800's, Bernheim and Liebeault came upon hypnosis as a treatment for physical and functional diseases, after one of Berheim's patients attributed her effective sciatica cure to hypnotic imagery. Bernheim and Liebeault began the most comprehensive study of hypnosis at the time, attempting to determine when and how hypnosis could be successfully applied. Once again, hypnosis lost favor to the effective new technological and medical advances of the period. Stronger emphasis was placed upon physical treatments for effective outcomes rather than psychological treatments (which was not an organized science at the time). This attitude continues today, although in the past several decades hypnosis has seen a revival of interest (Hall, 1986).

In 1990, Evans investigated the possible ways in which hypnosis effectiveness varies according to different types of pain (Evans, 1990). He determined that the style of hypnosis was more important than the type of pain. For acute pain, he suggested hypnotic suggestions focusing on anxiety-reduction and emphasis on minimizing the importance of the pain. For chronic pain, Evans suggested directly confronting the pain under hypnosis, dealing with both the pain's physical and psychological effects on the patient (Evans, 1990).

The most common psychological explanation for how hypnosis works is based upon a dissociation model. This model has been seen in patients with multiple personality disorder. Dissociation eliminates pain by placing it in a sort of psychological storage area, away from the primary consciousness of the patient. This model of dissociation is commonly referred to as the "hidden observer" model of cognition.

Watkins and Watkins (1990) suggested that the dissociation which occurs in multiple personality patients can be analogously induced in normal hypnosis patients. They referred to the dissociation as the use of an "ego state", and that in a normal person this state is malleable, as seen in varying mood states. In some moods, we are susceptible to do things which in other moods we are not. It is when this ego state is faulty that it breaks off into the "hidden observer" model. But hypnosis can induce placement of pain into a "covert" ego state which is hidden away. Because of this model, it is noted that the pain is still there, it is simply tucked away so that it is not dealt with The pain, however may resurface later in an undesirable form, such as a nervous habit or fear. So far, no support to this resurfacing theory has been shown (Watkins & Watkins, 1990).

The physiological explanations for the mechanism by which hypnosis controls pain management are even less understood than the psychological models. This avenue of study has not been pursued by many researchers, and almost nothing is known in this area.

Spiegel, et al, found a very conclusive physiological effect of hypnosis on pain management (1989). They determined that the neurophysiological amplitude of hypnotized subjects who were given pain-blocking imagery were significantly reduced in comparison to non-hypnotized subjects. They use this phenomenon to propose that there is, in fact, a definable neurophysiological basis for pain blockage via hypnosis. This would imply that hypnosis provides a measurable chemical inhibitory effect on pain conduction.

Weinstein and Au noticed that norepinephrine levels were significantly higher during angioplasty of hypnotized patients in comparison to non-hypnotized controls (Weinstein & Au, 1991). Consistent with that result is the knowledge that noradrenergic antagonists have inhibitory effects on REM sleep (Carlson, 1991). Because norepinephrine has an effect on sleep states, it is therefore possible that hypnosis increases these levels due to its similarity to an REM state of sleep. Unfortunately, endorphins are the neurotransmitter most frequently recognized as pain blockers. Research involving injection of a noradrenergic antagonist in hypnotized patients could lead to a more conclusive theory involving norepinephrine's role in hypnosis pain management.